Testosterone but not cortisol concentrations in hair correlate between mothers and their prepubertal children under real-life stress conditions.

The aim of the present study is to test the hypothesis that there is an association between the neuroendocrine state, reflected by testosterone and cortisol concentrations in hair, of the mother and her child under difficult real-life stress conditions (COVID-19 pandemic). The research sample consisted of 45 healthy mothers and their prepubertal children (7 - 11 years) of both sexes. The hair samples of mother-child dyads were collected twice to obtain cumulative stress hormone concentrations from April till the end of June and July till the end of September 2020. Thus, 90 mother-child pairs were analyzed. The results showed that both cortisol and testosterone concentrations were significantly higher in the hair of mothers compared to those in their children. The results of cortisol concentrations in hair do not support the hypothesis stated above. In line with our hypothesis are the results of hair testosterone measurements showing a positive correlation between testosterone concentrations in mothers and their children. With respect to the known relationship of testosterone with aggressive behavior, an important finding is that above-mentioned correlation was particularly strong in women with intense subjective feelings of anger in the investigated three months period. Women with strongly prevalent subjective feelings of sadness failed to show a significant correlation between hair cortisol concentrations in mothers and their children, in spite of the known relationship of cortisol to depressive mood. It may be suggested that chronic testosterone secretion reflects the association between the neuroendocrine function of the mother and her child under real-life stress conditions.

Cardiovascular and sympathetic responses to a mental stress task in young patients with hypertension and/or obesity.

Present study was aimed to investigate sympathetic responses to mental stress with hypothesis that the presence of obesity in patients with hypertension has a modifying effect. Young male subjects, 8 with hypertension grade I, with BMI 25 kg/m(2) (HT), 10 with hypertension grade I, and BMI 30 kg/m(2) (HT OB), 14 healthy controls with BMI 30 kg/m(2) (OB), and 13 healthy controls with BMI 25 kg/m(2) (C) underwent the Stroop test. ECG was recorded continuously to evaluate heart rate variability (HRV). Blood pressure (BP) and catecholamine concentrations were measured at baseline, at the end of mental stress test and 15 min thereafter. Patients with HT demonstrated increased adrenaline concentrations and enhanced stress-induced noradrenaline release compared to that in healthy controls. In obese subjects, stress-induced increase of systolicBP was lower compared to lean individuals. Stress exposure induced a significant rise in the low frequency power component of HRV, however the increase was lower in the HT OB group compared to C. Obesity in patients with hypertension did not lead to a different reaction in comparison with lean hypertensive subjects. The present data demonstrate higher sympathoadrenal activity in early-stage of hypertension. Obesity is connected with higher resting systolicBP and modifies the HRV response to mental stress.

Neuroendocrine and cardiovascular parameters during simulation of stress-induced rise in circulating oxytocin in the rat.

Physiological functions of oxytocin released during stress are not well understood. We have (1) investigated the release of oxytocin during chronic stress using two long-term stress models and (2) simulated stress-induced oxytocin secretion by chronic treatment with oxytocin via osmotic minipumps. Plasma oxytocin levels were significantly elevated in rats subjected to acute immobilization stress for 120 min, to repeated immobilization for 7 days and to combined chronic cold stress exposure for 28 days with 7 days immobilization. To simulate elevation of oxytocin during chronic stress, rats were implanted with osmotic minipumps subcutaneously and treated with oxytocin (3.6 microg/100 g body weight/day) or vehicle for 2 weeks. Chronic subcutaneous oxytocin infusion led to an increase in plasma oxytocin, adrenocorticotropic hormone, corticosterone, adrenal weights and heart/body weight ratio. Oxytocin treatment had no effect on the incorporation of 5-bromo-2-deoxyuridine into DNA in the heart ventricle. Mean arterial pressure response to intravenous phenylephrine was reduced in oxytocin-treated animals. Decrease in adrenal tyrosin hydroxylase mRNA following oxytocin treatment was not statistically significant. Oxytocin treatment failed to modify food intake and slightly increased water consumption. These data provide evidence on increased concentrations of oxytocin during chronic stress. It is possible that the role of oxytocin released during stress is in modulating hypothalamic-pituitary-adrenocortical axis and selected sympathetic functions.